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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ictal bradycardia is rare and its localising value is debated. Bradyarrhythmias are, however, important because of their potential connection to sudden death and ability to affect clinical seizure manifestations. Cerebral hypoperfusion induces loss of consciousness, at times with myoclonic jerks, whose clinical differentiation from a generalised convulsive seizure may prove difficult. Two invasive and five surface monitored seizures recorded over two years in a 51 year old woman with post-traumatic epilepsy characterised by seizure-triggered asystole were analysed. All seven seizures showed left temporal onset. Both intracranially recorded events started in the left anterior hippocampus/amygdala, spreading to the contralateral hippocampus in 35 and 25 seconds. Within 10 seconds an electrocardiogram showed asystole lasting 21 and 28 seconds, associated with suppression of recorded cerebral electrical activity, except a polyspike suppression pattern remaining in the hippocampi. Clinically, the patient, concomitantly with the cerebral suppression, developed myoclonic twitches of the limbs. A dual chamber cardiac pacemaker was implanted; at 11 months follow up, the patient has experienced only infrequent partial seizures, with none involving falls or shaking. Left temporal lobe seizures produced convulsive syncope initiated by ictal asystole. These observations suggest that intertemporal spread is necessary, though not sufficient, to produce bradycardia and asystole. Furthermore, pacemakers may decrease seizure severity, as well as potentially protect against malignant bradyarrhythmias.
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PMID:Ictal asystole with convulsive syncope mimicking secondary generalisation: a depth electrode study. 1589 20

Basic science studies of the human brain have supported the cortical representation of cardiovascular responses, including heart rate variability. Clinical observations of ictal bradyarrhythmia may be mechanistically explained by the influence of the central autonomic network, although the localization and lateralization issues need to be considered in the light of patterns of seizure spread, hand dominance, and presence of lesions. Ictal bradyarrhythmia also offers a mechanistic explanation of sudden unexpected death in epilepsy (SUDEP), though it may explain only some but not all cases of SUDEP. The missing links are (1) clinical evidence of common factors shared by patients with ictal bradyarrhythmia and patients who die from SUDEP, (2) evidence of arrhythmia as a risk factor for SUDEP from epidemiological studies, and, (3) determination of the importance of ictal bradyarrhythmia in SUDEP with respect to other proposed mechanisms including apnea and intrinsic cardiac abnormalities. There remains a need to review the seizure mechanisms in cases of SUDEP and to step up the amount of concurrent ECG/intracranial EEG analysis in both ictal bradyarrhythmia and SUDEP cases.
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PMID:Finding the missing link between ictal bradyarrhythmia, ictal asystole, and sudden unexpected death in epilepsy. 1680 68

The cortical control of the autonomic system may account for the clinical phenomenon of ictal asystole which, in turn, has been speculated to be a potential mechanism for sudden unexpected death in epilepsy (SUDEP). We report an 18-year-old patient with frontal lobe epilepsy who had intracranial electrode placement showing bifrontal seizure-onset. This patient received electrical stimulation to the left cingulate gyrus and developed cardiac asystole within 3 seconds of electrical stimulation. Intracranial monitoring showed epileptiform discharges in the left frontal polar, frontal lateral and interhemispheric electrodes. We suggest that the left cingulate gyrus, as part of the central autonomic network, may mediate bradyarrhythmia through the vagal pathway. There remains the possibility that other brain regions were also involved due to the time lag between asystole and epileptiform discharges, and the lack of intracranial exploration in the mesial temporal and insular regions. [Published with video sequences].
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PMID:Asystole induced by electrical stimulation of the left cingulate gyrus. 1730 16

The autonomic consequences of seizures can be severe. Death can follow from autonomic overactivity that causes a parasympathetically mediated bradyarrhythmia. We studied the cardiovascular consequences of unilateral and bilateral stimulation of the distal segments of transected vagus nerve in rats anesthetized with urethane. The range of stimulation rates tested is comparable to the firing rates observed in vagus nerve during seizures. There was a consistent inverse relation between stimulus rate and heart rate with nodal block appearing at 5-10 Hz and minimum HR levels (cardiac standstill) occurring at 50 Hz. Cardiac standstill could last many seconds. Blood pressure during VNS was maintained during lower frequency VNS, but collapsed at frequencies > or =20 Hz to dramatically impair ventricular filling. Recovery of heart rate and blood pressure after VNS was rapid. In the presence of sympathetic co-activation (pharmacological or hypercapnia and/or hypoxia), mean arterial pressure was better maintained and there was much better ventricular filling, but cardiac performance was worse (e.g. ejection fraction derived from echocardiography). The combination of sympathetic and parasympathetic overactivity was sometimes associated with prolonged (> or =20 s) apneic periods during VNS. We conclude that an abrupt increase in parasympathetic activity on the order of 5 times the background of parasympathetic tone can produce transient bradyarrhythmias, and increases on the order of 20 times can produce cardiac standstill, sometimes accompanied by apnea. Our findings suggest that parasympathetically mediated bradyarrhythmia must be accompanied by airway obstruction to sustain parasympathetic overactivity and produce hypoxia to ultimately cause death.
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PMID:Vagus nerve stimulation-induced bradyarrhythmias in rats. 1965 41

Epileptic seizures are accompanied by changes in autonomic function that in turn influence the cardiovascular system (hypertension and bradyarrhythmia). We have studied possible cardioprotective activity (during the ictal state in conscious animals) of valproic acid, nifedipine, and verapamil, alone and in combination, during pentylenetetrazole (PTZ)-induced seizures. Telemetry system was used for recording EEG, blood pressure, and heart rate in conscious, freely moving rats during seizures. We observed that PTZ-induced seizures were accompanied by hypertension and bradyarrhythmia. Pretreatment with valproic acid did not block seizure-induced hypertension and bradyarrhythmia. Nifedipine alone and in combination with valproic acid blocked seizure-induced hypertension and bradyarrhythmia significantly. We also observed that pretreatment with verapamil alone and in combination with valproic acid did not block seizure-induced hypertension and bradyarrhythmia significantly. Our results suggest that pretreatment with nifedipine alone or in combination with valproic acid provides protection against seizure-induced hypertension and bradyarrhythmia.
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PMID:Epileptic seizure-induced hypertension and its prevention by calcium channel blockers: a real-time study in conscious telemetered rats. 1976 81

Vagus nerve stimulation (VNS) for medically refractory seizures has been an approved therapy by the Food and Drug Administration since 1997, with additional approval as an adjunct therapy for major depression granted in 2005. Potential applications for VNS therapy in obesity, neuropsychiatric disorders, and chronic pain syndromes are under investigation. Bradyarrhythmias, including asystole, may occur during VNS device placement or as a delayed complication. A peritracheal hematoma may develop following VNS device placement, necessitating emergent management. Other respiratory complications may include vocal cord movement abnormalities with potential for aspiration. Vagus nerve stimulation results in sleep-related breathing pattern changes, with an associated increase in the number of obstructive apneas and hypopneas in both children and adults, which may impact perioperative care.
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PMID:Intraoperative and perioperative complications with a vagus nerve stimulation device. 2040 10

Autonomic dysfunction during seizures can induce bradyarrhythmia via efferent vagal overactivity. We studied cardiovascular, brain blood flow, and electroencephalographic consequences of vagal stimulation during seizures in rats. Efferent vagal stimulation reduced seizure activity, completely suppressing it at high frequencies, by reducing heart rate, arterial pressure, and cortical blood flow. Afferent vagal activation was more variable, and the highest stimulation frequencies also appeared to reduce cortical blood flow. We conclude that efferent vagal activity can arrest ongoing seizure activity by ultimately decreasing hippocampal blood flow. Afferent vagal activity (which does not occur during seizures) may have a similar action.
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PMID:Efferent and afferent vagal actions on cortical blood flow and kainic acid-induced seizure activity in urethane anesthetized rats. 2051 Jun 56

Mepivacaine is a potent local anaesthetic and used for infiltration and regional anaesthesia in adults and pediatric patients. Intoxications with mepivacaine affect mainly the CNS and the cardiovascular system. We present a case of accidental intravenous mepivacaine application and intoxication of an infant resulting in seizure, broad complex bradyarrhythmia, arterial hypotension and finally cardiac arrest. The patient could be rescued by prolonged resuscitations and a rapid initiation of ECMO and survived without neurological damage. The management strategies of this rare complication including promising other treatment options with lipid emulsions are discussed.
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PMID:ECMO for Cardiac Rescue after Accidental Intravenous Mepivacaine Application. 2296 72

We present the case of a 7-year old boy with traumatic brain injury who received propofol during 38 h. Thirty-six hours after cessation of propofol infusion asystole occurred. After immediate mechanical and medical resuscitation, unreactive dilated pupils were observed. The following computed tomography scan revealed a generalized brain edema with transtentorial herniation. Prolonged bradyarrhythmia, rhabdomyolysis, and peracute renal failure were observed. Despite immediate craniectomy, barbiturate treatment, hemofiltration, and recovery of appropriate cardiac function, the patient died four days after discontinuation of propofol. In this case, metabolic acidosis, cardiac failure, rhabdomyolysis, and renal failure are in accordance with the symptoms of propofol infusion syndrome (PRIS), while seizure, brain edema, and transtentorial herniation could be caused by traumatic brain injury. However, it may be assumed that the entire clinical picture was caused by PRIS. This view could be explained by a common loss of function of ryanodine receptors in patients presenting with PRIS.
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PMID:Rare, potentially fatal, poorly understood propofol infusion syndrome. 2476 78

Anti-N-methyl-d-aspartate receptor encephalitis (anti-NMDARE) is autoimmune encephalitis primarily affecting young adults and children. First described about a decade ago, it frequently manifests as a syndrome that includes progressive behavioral changes, psychosis, central hypoventilation, seizures, and autonomic instability. Although cardiac arrhythmias often accompany anti-NMDARE, the need for long-term electrophysiological support is rare. We describe the case of NMDARE whose ICU course was complicated by progressively worsening episodes of tachyarrhythmia-bradyarrhythmia and episodes of asystole from which she was successfully resuscitated. Her life-threatening episodes of autonomic instability were successfully controlled only after the placement of a permanent pacemaker during her ICU stay. She made a clinical recovery and was discharged to a skilled nursing facility after a protracted hospital course.
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PMID:Profound Autonomic Instability Complicated by Multiple Episodes of Cardiac Asystole and Refractory Bradycardia in a Patient with Anti-NMDA Encephalitis. 2719 Jun 63


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